期刊
NATURE REVIEWS DRUG DISCOVERY
卷 8, 期 12, 页码 969-981出版社
NATURE PUBLISHING GROUP
DOI: 10.1038/nrd3031
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资金
- NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES [P01AI073489] Funding Source: NIH RePORTER
- NIAID NIH HHS [P01 AI073489, P01 AI073489-020003] Funding Source: Medline
Classical zinc-dependent histone deacetylases (HDACs) catalyse the removal of acetyl groups from histone tails and also from many non-histone proteins, including the transcription factor FOXP3, a key regulator of the development and function of regulatory T cells. Many HDAC inhibitors are in cancer clinical trials, but a subset of HDAC inhibitors has important anti-inflammatory or immunosuppressive effects that might be of therapeutic benefit in immuno-inflammatory disorders or post-transplantation. At least some of these effects result from the ability of HDAC inhibitors to enhance the production and suppressive functions of FOXP3(+) regulatory T cells. Understanding which HDACs contribute to the regulation of the functions of regulatory T cells may further stimulate the development of new class-or subclass-specific HDAC inhibitors with applications beyond oncology.
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